Thanks to Joost G. Wouters for the alert to this nonsense:
1) Michael White in Pacific Standard magazine flatly states that “Epigenetics Is Not Revolutionizing Biology.”
2) Adrian Bird points out in the journal Cell that many of the field’s assumptions and promises remain unproven and are perhaps excessive.
1) White’s article sketches the field’s promise and hype, from questionable epigenetic diets and wild claims about controlling genes with your thoughts. He follows with a summary of epigenetics, then runs through a list of his ridiculous qualms about the field. White paraphrases, “the hype has outrun the science” at a time when serious scientists are Combating Evolution to Fight Disease by integrating everything known about epigenetic links between metabolic networks and genetic networks.
“…scientists have long been aware that our genes aren’t chiseled in stone—they are in a constant dialogue with our environment,” White says. Obviously, he means “gene expression” is not chiseled in stone because the epigenetic landscape is linked to the physical landscape of DNA in all organized genomes by RNA-mediated events. But that point gets glossed over in his excited attack on everything he thinks is not supported by what is currently known about physics, chemistry, and molecular epigenetics.
He doesn’t like the fact that many of the field’s supposed findings for humans — say, that you can inherit specific fears — are based entirely on animal studies, although that is the basis for nearly everything incorporated into today’s medical practice. And of course, pseudoscientists make an issue of whether epigenetic marks are truly a cause or an effect of changes wrought on gene expression by other factors. They have no concept of how the epigenetic landscape is linked via sensory input to the physical landscape of DNA.
White says, “There is no reason to believe that drugs, treatments, or health advice that target these DNA markings will be unusually effective compared to therapies that aren’t specifically epigenetic.” He concludes that it’s overall a good development, but perhaps we need to mind the hype. But see: Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing. It links what is also known about nutritional epigenetics to biologically-based cause and effect in species from microbes to man.
2) Edinburgh University’s Adrian Bird writes in the journal Cell about the overblown idea that biology is undergoing some sort of revolutionary turmoil, only part of which is due to epigenetics.
“So that’s not *junk* DNA?”, “What’s the definition of a gene?”, and “What how much effect does long, non-coding RNA actually have?” These issues consume the article’s first half, but he really gets rolling later. We have good evidence of transgenerational epigenetic inheritance in precious few places, which include C. elegans inheritance of RNA-based viral resistance. That Swedish “hunger winter” stuff is interesting, but hardly rigorous just yet.
And anyway, says Bird, why would passing along diabetes or obesity — as with the hunger winter — be some sort of adaptive mechanism? After all, perhaps the apparently inherited traits just result from malfunctions in the slate-wiping that every animal seems to do early in development.’ My comment: Viral resistance is nutrient-dependent and in animals it is controlled by the metabolism of nutrients to species-specific pheromones that control the physiology of reproduction. Thanks to Joost for permission to use pars of his original introduction, with alterations. He wrote: “No permission required on my part…” Most links are in the PSMAG article itself. Check out those articles here! See also: Serving epigenetics before its time and Scrutinizing the epigenetics revolution
Excerpt:Cancer, for example, is caused by genetic mutations that can’t be undone, but it is also characterized by abnormal epigenetic marks, which can potentially be reversed. Researchers have struggled for years, with little success, to fix our genetic print by repairing mutations with gene therapy. But in some cases we may not need to repair mutations if we can re-work the epigenetic pencil marks instead. Excerpt: Many of the boldest claims being made about the relationship between epigenetics, health, and our environment are based only on evidence from animal studies, and thus are, at best, premature. In fact, much of the recent research in epigenetics hasn’t turned up anything fundamentally new. Excerpt: Epigenetic marks are a consequence of changes in the activity of our genes in response to our health, our environment, and our social experiences, but they are not the underlying cause of those changes. My comment: Simply put, if you are a social scientist, admitting that the epigenetic landscape is directly linked to the physical landscape of DNA via RNA-directed DNA methylation and RNA-mediated amino acid substitutions in species from microbes to man is like admitting you have always been a biologically uninformed theorist who knows nothing about top-down causation of the control of biodiversity by RNA-mediated events. That explains why you may have attributed biodiversity to mutations and/or natural selection and evolution. It does not explain how anyone who is biologically informed could also ignore what is known about physics and chemistry and claim that: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” (p. 199) Mutation-Driven Evolution
August 29, 2013 Excerpt: …studies in C. elegans show that epigenetic alterations in gene expression are only passed to the next generation when a protein that strips a chemical mark from chromatin is mutated ( Katz et al., 2009). Transgenerational epigenetic inheritance in these mutants may be exemplary, but its corollary is a decline in fertility, ending with collapse of the lineage. Excerpt: Despite the shortage of convincing evidence, the idea that the consequences of human life experience are epigenetically transmitted across generations has gained remarkably wide currency. My comment: That explains the advent of personalized medicine, which links metabolic networks to genetic networks via the conserved mechanisms of molecular epigenetics. For example, we detailed what was known about biologically-based top-down causation and RNA-mediated control of cell type differentiation in a section of our 1996 Hormones and Behavior review: From Fertilization to Adult Sexual Behavior. Since then, many other serious scientists have continued to add details that extend nutrient-dependent pheromone-controlled sex differences in cell types to cell type differentiation in all cells of all individuals of all species via the conserved molecular mechanisms that link physics, chemistry, and biology to the sun’s biological energy. For example, viral microRNAs are linked from entropic elasticity to accumulated mutations and physiopathology. Nutrient-dependent microRNAs link the anti-entropic epigenetic effects of the sun’s biological energy to DNA repair and the physiology of reproduction, which enables fixation of the nutrient-dependent amino acid substitutions that stabilize RNA-mediated protein folding in the organized genomes of species from microbes to man.
The biophysically constrained chemistry of protein folding links the molecular epigenetics of cell type differentiation from the interactions of sunlight and water to the origins of cell type creation and to the differentiation of all cell types in all individuals of all genera.
Rejuvenation Biotechnology 2014
“Regulating a Damage Repair Approach to Cure the Diseases of Aging” (55 minutes) Panel Discussion (August 23, 2014, 12:30pm)
Making sense of amino acid sensing links nutrient-dependent RNA-directed DNA methylation via amino acid substitutions to cell type differentiation in all cell types of all tissue in all organs of all organ systems in mammals via blood cell circulation. Dobzhansky (1973) placed this into the context of primate biodiversity. He wrote: “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.” (p. 127)
